human phys exam 2 Flashcards
1
Q
types of muscles
A
skeletal
cardiac
smooth
2
Q
skeletal muscles
A
large
multinucleate
one muscle fiber
voluntary muscle controlled by somatic efferent neurons
3
Q
cardiac muscles
A
smaller than skeletal
uninucleate
striated
all cells are connected by intercalated disks
involuntary muscle controlled by autonomic motor neurons
4
Q
smooth muscle
A
small
no striations
uninucleate
involuntary muscle controlled by autonomic motor neurons
5
Q
muscle fiber
A
muscle cell
called syncitum
6
Q
sarcolemma
A
cell membrane in skeletal muscle
7
Q
sarcoplasm
A
cytoplasm in skeletal muscles
8
Q
sarcoplasmic reticulum
A
endoplasmic reticulum in muscles
stores calcium
9
Q
myofibrils
A
bundles of contractile proteins
each muscle fiber has myofibrils
10
Q
contractile proteins in muscle fibers
A
actin
myosin
troponin
tropomyosin
11
Q
actin
A
thin filament
5 nm
12
Q
myosin
A
thick filament
15 nm
13
Q
t- tubules
A
extensions of sarcolemma that associate with ends of sarcoplasmic reticulum
allows action potential to go deep into muscle
14
Q
a band
A
anywhere there is myosin
(can be actin)
15
Q
h zone
A
only myosin
16
Q
i band
A
only actin
17
Q
m line
A
where myosin is anchored
18
Q
z disk
A
where actin is anchored
19
Q
sarcomere
A
z disk to z disk
3 um in lenght
20
Q
titin
A
huge protein
like a spring
gives passive tension to muscle
21
Q
myosin molecule
A
each molecule has 2 myosin heads
hinge region allows molecule to pivot
22
Q
during contraction
in sarcomere
A
sarcomere shortens
length of actin and myosin DO NOT change!
there is just more overlap between actin and myosin
- i band gets shorter
- h zone gets shorter
23
Q
cross bridge cycle in skeletal muscle
A
- ATP binds to myosin, causes myosin to leave rigor state and unbind from actin
- myosin hydrolyzes (ATPase activity) ATP to ADP and inorganic phosphate (high energy state). This causes myosin hinge point to pivot
- myosin head swings over and binds weakly to a new molecule (high energy state). Release inorganic phosphate
- release of inorganic phosphate causes Power Stroke. myosin head rotates and pushes actin past it
- this causes sarcomer to get shorter
- end of power stroke, myosin releases ADP and is still binded to actin (rigor state)
24
Q
what prevent cross bridge from happening
(why arent our muscles always contracting)
A
tropomyosin lays on top of binding site between actin and myosin, prevents myosin to bind to actin and complete power stroke
(this is after myosin hydrolyzes ATP)
25
How is tropomyosin moved to allow contraction?
when cytosilic calcium binds to troponin, it causes conformation change to troponin which pulls tropomyosin away from the binding site
this allows myosin to bind to actin and complete power stroke
26
excitation-contraction coupling
1. somatic motor neurons release ACh
2. Na+ enters through ACh receptor --> initiates action potential (depolarizes)
3. action in t-tubule alters conformation of DHP receptor
4. DHP opens Ryr Ca+ channels, releases Ca into cytoplasm
5. Ca binds to troponin
6. myosin completes power stroke
27
how does relaxation occur?
IN SKELETAL MUSCLES
calcium needs to be removed
1. Sarcoplasmic Ca-ATPase (SERCA) pumps calcium back into sarcoplasmic reticulum against concentration gradient
2. decrease in calcium causes calcium to unbind from troponin
3. tropomyosin can rebind to myosin binding site
relax
28
3 roles of ATP in skeletal muscle contraction
1. myosin hydrolyzes ATP, provides energy for cross bridge
2. binding of ATP to myosin dissociates actin and myosin
3. hydrolysis of ATP by Ca-ATPase provides energy for active transport of calcium back into SR
29
motor unit
motor neuron and muscle fiber it innervates
- there are way more muscle fibers than neurons
- each muscle fiber is innervated by a single neuron
- each neuron innervates multiple muscle fibers
30
latent period
twitch is delayed from action potential because the time it takes for calcium to increase in sarcoplasm and interact with troponin
twitch contraction lasts longer than action potential because it takes time for calcium to pumped back into SR
31
temporal summation skeletal muscle
2 action potential stimuli are close in time, can cause a larger tiwitch
twitch lasts much longer than action potential
32
isotonic contraction
muscle moves the load and gets shorter
33
isometric contraction
muscle forces balances out the weight, so the muscle doesnt move the load
34
lengthening contraction
the weight wins, so despite the muscle trying to contract it still gets shorter
35
contraction steps
1. muscle at rest
2. isometric contraction: muscle hasn't shortened (sarcomeres have shortened but elastic elements stretch = length is same)
3. isotonic contraction (elastic components are fully stretched but still more overlap of actin and myosin = muscle shortens)
36
slow oxidative muscle fiber
- darker because they contain myoglobin
- use oxidative phosphorylation (lot of ATP)
- resist muscle fatigue
- small diameter: allow oxygen can go into muscle
37
fast oxidative muscle fiber
- mediam diameter fibers
- contain less myoglobin
- can use glyolysis and oxidaive phosphorylation
- produce greater amount of tension than slow but will fatigue (not as quickly as fast glycolytic)
38
muscle fiber recruitment
recruit fibers that are least energetically expensive (slow oxidative)
39
similarities between skeletal and smooth muscle
specialized for contraction
contract by sliding myosin and actin
calcium is important regulator
contraction requires ATP
40
single unit smooth muscle
gap junctions connect cytoplasm of 2 cells so ATP can travel
contract in synchronous because of gap junction
41
multi unit smooth muscle
not connected by gap junction but rather axons
more precise control
42
innervation of smooth muscle
autonomic nervous system
parasympathetic pathway
sympathatetic pathway
adrenal sympathetic pathway
43
innervation of skeletal muscle
somatic motor pathway
neuron releases acetylcholine, actins on nicotinic acetylcholine receptor (ligand gated) in skeletal muscle
44
parasympathetic innervation of smooth muscle
preganglionic: releases Ach acts on nicotininc receptor on ganglion
post ganglionic: releases Ach acts on g-protein (muscarinic)receptors in smooth muscle
45
sympathetic innervation of smooth muscle
preganglionic: releases Ach acts on nicotinic receptor on ganglion
postganglionic: releases norepinephrine acts on adrenergic receptors (g-coupled)
46
adrenal sympathetic innervation of smooth muscle
preganglionic: releases Ach acts on nicotinic receptors in adrenal medulla
releases epinephrine into bloodstream
47
dense bodies
where actin is anchored in smooth muscles
when smooth muscle contracts, they get closer to each other
48
contraction in smooth muscle
1. Ca enters cell from SR
2. Ca binds to calmodulin (CaM)
3. CaM activates myosin light chain kinase (MLCK)
4. MLCK phosphorylates light chain in myosin head --> increases myosin ATPase activity
5. active myosin crossbridges slide along actin and create muscle tension
49
relaxation in smooth muscle
calcium needs to be removed!
1. Ca-ATPase pumps Ca back into CR
2. Ca unbinds from CaM, decreases MLCK activity
3. myosin phosphatase removes phosphate from myosin, decreases myosin ATPase activity
4. less myosin ATPase activity = decreased muscle tension
50
latch mechanism
smooth muscle can maintain contraction with minimal expenditure of energy
51
tension in smooth muscle
tension development is slowest
cross bridge cycle works more slowly and is not constant
52
factors influencing smooth muscle activity
- spontaneous electrical activity
- norepinephrine and acetylcholine)
- hormones
- stretch
- paracrines
53
goal of cardiovascular system
maintain delivery of oxygen and nutrients
removal of wastes from tissue
54
total blood volume
about 5 liters
55
plasma volume
55%
56
white cell volume
less than1%
57
red cell volume (hematocrit)
45%
58
red cell count
5 million
59
white cell count
several thousand
60
hemoglobin volume
15 g/dL
61
plasma
mostly water
gases, nutrients, wastes
hormones
proteins (7%)
62
proteins in plasma
albumin 4.5 (carrier protein)
globulins 2.5
fibrinogen 0.3
63
Na+ concentration
145 mM
64
K+ concentration
4 mM
65
Ca2+ concentration
2.5 mM
66
CO2 concentration
2 ml/100ml (1 mM)
67
O2 concentration
0.2ml/100ml (0.1 mM)
68
N2 concentration
0.9ml/100ml(0.5mM)
69
glucose concentration
100 mg/100ml (5.6 mM)
70
erythrocytes
red blood cells
purpose: deliver oxygen
7 microns in diameter (capillaries are same)
2 mil hemoglobin per RBC (15g/100ml)
no nucleus or ribosomes
71
erythropoietin
hormone released by kidney
stimualtes production of red blood cells through negative feedback
decreased O2 in kidneys
kidneys release erythropietin
acts on bone marroe to increase production of hemoglobin
increase O2 delivery to kidney
72
anemia
decreased oxygen carrying capacity of blood
can be related to too few red blood cells
or not enough hemoglobin per RBC
73
iron and blood
iron is essential for RBC synthesis
74
leukocytes vs erythrocytes
leukocytes are larger
less leukocytes than erythrocytes
75
general organization of cardiovascular system
right heart pumps to lungs (pulmonary circuit) which pumps to left heart
left heart pumps to tissues (systemic circuit)
76
blood flow
pressure/resistance
increase pressure, increase flow
decrease resistance, increase flow
77
resistance to flow
viscocity
length
radius (major factor)
78
hemostasis
clotting process
essential for preventing blood loss from damaged vessels
79
valves
allow for unidirectional flow
passive due to pressure
80
aortic valves
tricuspid (right)
bicuspid/mitral (left)
prevent blood from flowing backwards from the ventricle into atria during ventricular contraction
81
semilunar valves
pulmonary (right)
aortic (left)
prevent blood from flowing backwards from the aorta and pulmonary artery into ventricles
82
pericardium
sac of connective tissue around pericardial fluid
83
endocardium
chambers of heart are lined with epithelium
84
myocardium
heart muscle
85
cardiac muscle arrangement
spiral--> allows ventricular contraction to squeeze blood upward
86
intercalated disks cardiac muscle
contain desmosomes that transfer force from cell to cell
also contains gap junctions that allow electrical signals to pass rapidly from cell to cell
87
types of cardiac cells
contractile
autorhythmic (pacemaker)
88
contractile cells
muscle cells
myocites
89
pacemaker cells
in right atrium in SA node
spontaneous
90
cardiac myocyte contraction
1. action potential spreads
2. voltage gated Ca channels open
3. Ca causes Ca release from RyR channels
4. local release causes Ca spark
5. summed Ca sparks create Ca signal
6. Ca ions bind to troponin = initiate contraction
91
cardiac myocyte relaxation
1. calcium unbinds from troponin
2. Ca pumped back into SR
3. Ca is exchanged with Na
4. Na gradient is maintained by Na-K-ATPase
92
ventricular myocyte action potential
1. rest: 90 mV
2. depolarizing phase: increase Na
3. plateau phase : decrease Na and K, increase Ca (250 msec)
4. repolarizing phase: increase K, decrease Ca
93
SA node pacemaker action potential
1. rest: -60 mV
2. slow influx of Na+ (funny current)
3. depolarization: rapid influx of Ca
4. repolarization: increase K+ to rest -60 mV
100 cycles/min
94
SA node pacemaker action potential steps
1. SA node depolarizes
2. electrical activity goes to AV node
3. depolarization spreads slowly across atria
4. depolarization moves rapidly through ventricular system
5. depolarization wave spreads from apex
95
skeletal muscle
membrane potential
events leading to threshold
rising phase of action potential
repolarization phase
hyperpolarization
duration
refractory period
-90 mV
Na+ entry through Ach channels
Na+ entry
rapid, caused by K+ efflux
due to K+ efflux and high K_ permeability
short (1-2msec)
brief
96
contractile myocardium
membrane potential
events leading to threshold
rising phase of action potential
repolarization phase
hyperpolarization
duration
refractory period
-90 mV
depolarization enters via gap junctions
Na+ entry
extended plataeu caused by Ca+ entry
no hyperpolarization
extended (200 msec)
long because resetting Na+ gets delayed until end of ap
97
autorhythmic myocardium (Pacemaker)
membrane potential
events leading to threshold
rising phase of action potential
repolarization phase
hyperpolarization
duration
refractory period
-60 mV
net Na+ entry through funny channels, reinforced by Ca entry
Ca2+ entry
rapid, caused by K+ efflux
no hyperpolarization
150 msec
no refractory period
98
cardiac cycle
late diastole
atrial systole
isovolumetric ventricular contraction
ventricular ejection
isovolumic ventricular relaxation
99
late diastole
step 1
both sets of chambers are relaxed
ventricles fill passivley
100
atrial systole
step 2
atrial contraction forces small amount of additional blood into ventricles
101
isovolumic ventricular contraction
step 3
first phase of ventricular contraction
pushes AV valves closed
doesn't create enough pressure to open semilunar valves
102
ventricular ejection
step 4
ventricular pressure rises and exceeds pressure in arteries
causes semilunar vales to open and blood is ejected
103
isovolumic ventricular relaxation
step 5
ventricles relax and pressure decreases
blood flows back into cups of semilunar valves and they close
104
EDV
end diastolic volume
diastole is filling
105
ESV
end systolic volume
systole is pumping
106
stroke volume
amount of blood pumped by one ventricle during a contraction
end diastolic volume - end systoliv volume
107
cardiac outut
volume of blood pumped per unit time by left heaart
= heart rate x stroke volume
108
autonomic control of heart
- sympathetic and parasympathetic innervation of SA and AV node
sympathetic innervates ventricular muscle = regulates force of contraction
109
starling law
stroke volume increases as EDV increases
110
funny current
sodium leak
causes membrane to slowly depolarize until threshold of ca channels start action potential
111
EKG
measures heart rate, electrical signals, duration of ventricular diastole
112
arteries
large diameter
low resistance
distribute blood around body
compliant--> keep blood flowing during diastole (elastic recoil)
113
pulse pressure
systolic pressure minus diastolic pressure
114
mean arterial pressure
diastolic pressure + 1/3 pulse pressure
115
at factors influence pulse pressure
stroke volume
heart rate
arterial compliance
116
sphygmomanometry
measurement of arterial blood pressure
117
arterioles
major source of resistance
drop in pressure
decreased diameter increases resistance
increase resistance decreases flow
118
myogenic tone
muscle tone in arterioles
119
local mechanisms of myogenic tone
active hyperemia
flow autoregulation
120
active hyperemia
increase metabolites
decrease oxygen
increase dilation of arteroile
increase blood flow
121
flow autoregulation
decrease pressure
decrease flow
decrease o2, increase metabolies
dilate arteriole
restore normal blood flow
122
neural controls of myogenic tone
vasoconstrictors:
sympathetic nerves that release norepinephrine
vasodilators:
neurons that release nitric oxide
123
alpha receptors on muscles
constrictor
norepinephrine from sympathetic neurons
124
beta receptors on muscles
dilator
epinephrine from adrenal medulle
125
arteriole diameter control
release of norepinephrine
sympathetic releases norepinephrine and act on alpha receptor
causes blood vessel to constrict
(decrease NE cause dilate)
126
norepinephrine (a-recpetors)
role
source
type
vasoconstriction
baroreceptor and more
sympathetic neurons
neurotransmitter
127
vasopressin
role
source
type
vasoconstriction
increase blood pressure in hemorrhage
posterior pituitary
neurohormone
128
angiotensin II
role
source
type
vasoconstriction
increase blood pressure
plasma hormone
hormone
129
epinephrine (B-receptors)
role
source
type
vasodilation
increase blood flow
adrenal medulla
neurohormone
130
nitric oxide
role
source
type
vasodilation
local control blood flow
endothelium
paracrine
131
decrease O2, increase CO2
role
source
type
vasodilation
increase blood flow
cell metabolism
paracrine
132
adenosine
role
source
type
vasodilation
increase blood flow
hypoxic cells
paracrine
133
histamine
role
source
type
vasodilation
increase blood flow
mast cells
paracrine
134
natriuretic peptide (ANP)
role
source
type
vasodilation
reduce blood pressure
atrial myocardium
hormone, neurotransmitter
135
dicrotic notch
as blood pressure is falling, there is a little bump up
136
atherosclerosis
plaque build up
makes walls less compliant
increase pulse pressure
137
capillaries
site of exchange between circulatory system and interstitial fluid
small diameter but combined has large total cross sectionl area
= slowest velocity
138
continuous capillaries
leaky junctions
endothelial cell junctions allow water and small solutes to pass
139
fenestrated capillaries
have large pores
transcytosis brings proteins and macromolecules across endothelium
140
function of lymphatic system
return fluid to CVS
clearing proteins from interstitial fluid
absorb fat in intestine
immune system
141
edema
accumulation of fluid in interstitial fluid
142
what causes edema
- lymphatic drainage is compromised : accumulate fluid
- balance of pressure between capillary hydrostatic and somatic pressure may favor movement of fluid into interstitial space
143
what causes pressure favoring movement into interstitial space
- increased capillary pressure
- decreased plasma protein conc. (liver failure)
- increased interstitial fluid protein
144
venules and veins
return blood to heart
low resistance
pressure is low coming out of the capillaries
145
factors that assist with return of blood to heart
valves
skeletal muscle pump
respiratory pump
146
skeletal muscle pump
skeletal muscle contracts
squeeze veins in muscle
push blood out
valves make sure its towards heart
147
respiratory pump
breathing changes pressure in thoracic cavity
valves make sure pump blood toward heart
148
veins
low resistance
very compliant
stretch to accomodate blood volume
149
lymphatic system
series of tubes open at one end to interstitial fluid
small lymphatic vessels merge to larger vessels, which open into vena cava
lymph nodes throughout lymphatic system
3L/day of fluid lost from capillaries that enter lymphatic vessels, return to blood stream
150
lymph fluid
fluid found in vessels
fluid moves from interstitial fluid to small lymphatic vessels by passive pressure
valves ensure flow is unidirectional
151
lymph fluid
fluid found in vessels
fluid moves from interstwhy is blood flow through capillaries constantitial fluid to small lymphatic vessels by passive pressure
valves ensure flow is unidirectional
152
why is blood flow through capillaries constant?
resistance of arteries
153
pressure gradient in capillaries
diminishes along length of capillary because pressure falls due to resistance
154
baroreceptor reflex
negative feedback
increase blood pressure --> baroreceptors fire
decrease sympathetic output
increase parasympathetic output
155
tion of baroreceptors
carotid sinus
aortic arch
156
orthostatic hypotension
blood pressure decreases when standing
carotid and aortic receptors increase sympathetic output to vasoconstrict
increase resistance
increase blood pressure
157
angiotensin
produced in blood by renin (enzyme release in kidney)
kdieny acts on angiotensinogen (Made in liver)
158
angiotensin I
10 amino acid
generated from angiotensin
rapidly converted to angiotensin II
converted by ACE
159
ACE
angiotensin converting enzyme
found in membrane of epithelial cells in pulimonary capillaries
convert Ang 1 to Ang II
160
angiotensin II
8 amino acid
increase blood pressure
constrict arterioles
161
renin secretion
decreases arterial pressure
decreased renal perfusion
162
hemorrhage
blood loss
increase sympathetic activity
increase blood pressure
increase CO and resistance
163
hemorrhage
blood loss
increase sympathetic activity
increase blood pressure
increase CO and resistance
164
hypertension (high blood pressure)
fix
- beta1 antagonist (lower blood pressure by decreasing CO)
- lower ACE
- alpha antagonist: block sympathetic vasoconstriction
- calcium channel blockers: reduce vascular smooth muscle contraction
diuretics: reduce blood flow and CO
165
calcium source
skeletal vs smooth
skeletal: sarcoplasmic reticulum
smooth: extracellular
166
PQ interval (PR)
time required for atrial depolarization and action potential to reach ventricles
167
PQ segment
time for atrial depolarization to propagate through ventricles
168
ST segment
time between ventricular depolarization and repolarization
169
QT interval
time required for ventricular depolarization and repolarization
170
RR interval
accurate measure of the time of a single cardiac cycle
171
P wave
atrial depolarization
172
QRS
ventricular depolarization
173
T
ventricular repolarization
